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Biomedical subjects

K B Moore

Publications and source records attributed to K B Moore.

11 recordsLinked to original sources
PubMed2003

The albuminuric action of atrial natriuretic peptide is not modified by ACE-inhibition with perindopril in Type 2 diabetes.

AIMS: Atrial natriuretic peptide (ANP) increases urine albumin excretion (UAER) in humans with Type 1 diabetes. The aim of this study was to establish if ANP increases UAER in microalbuminuric subjects with Type 2 diabetes and to examine whether the albuminuric action of ANP was inhibited by pre-treatment with the ACE-inhibitor perindopril. METHODS: Seven microalbuminuric, normotensive males with Type 2 diabetes were entered into a randomised, double-blind, three-armed study of (i) intravenous infusion of ANP (0.25 microg/kg/min in 0.9% NaCl) after 3 weeks' pre-treatment with placebo, (ii) intravenous infusion of vehicle (0.9% NaCl only) after 3 weeks' pre-treatment with placebo, or (3) intravenous infusion of ANP (0.25 microg/kg/min in 0.9% NaCl) after 3 weeks' pre-treatment with perindopril, 4 mg daily. RESULTS: Baseline parameters were similar on all three study days. During the placebo/vehicle arm there was no change in urine flow rate (UFR, P=0.61), urine cyclic guanosine monophosphate (UcGMP P=0.48) or UAER (P=0.99). During the placebo/ANP arm there was a rise in UFR [13.7+/-2.8 (mean+/-sd) to 25.7+/-7.7 mL/min, P<0.001], UcGMP (60.0+/-36.6 to 160.8+/-118.5 micromol/mmolCr, P=0.045) and UAER [5.13 [2.4-11.6][median (range)] to 71.6 [21.6-175.1] mg/mmolCr, P<0.001]. Pre-treatment with perindopril did not alter the changes in UFR (P=0.63), UcGMP (P=0.46) or UAER (P=0.99) to infusion of ANP, compared with the placebo/ANP arm. CONCLUSION: ANP increases UAER in microalbuminuric patients with Type 2 diabetes and the albuminuric action of ANP is not inhibited by pre-treatment with the ACE inhibitor perindopril.

Adult↗
PubMed2001

Becoming glial in the neural retina.

During development of the vertebrate neural retina, multipotent stem cells give rise to retinal neurons as well as to Müller cells, the principal glial population in the retina. Recent studies have shed light upon the extracellular and intracellular signaling pathways that regulate Müller glial cell genesis. Emerging evidence demonstrates that activation of the Notch signaling pathway can play a role in regulating Müller cell development as well as gliogenesis in other parts of the central nervous system. Cyclin dependent kinase (CDK) inhibitors of the Cip/Kip subfamily are cell cycle regulators that can regulate progenitor proliferation during retinal development, but also regulate the proliferation of Müller glia when they become activated in response to stress or injury. Surprisingly this class of proteins can also promote the development of Müller glia. In this review we discuss the role of both Notch and the CDK inhibitors in regulating Müller cell development.

Animals↗
PubMed1999

Animal-vegetal asymmetries influence the earliest steps in retina fate commitment in Xenopus.

An individual retina descends from a restricted and invariant group of nine animal blastomeres at the 32-cell stage. We tested which molecular signaling pathways are responsible for the competence of animal blastomeres to contribute to the retina. Inactivation of activin/Vg1 or fibroblast growth factor (FGF) signaling by expression of dominant-negative receptors does not prevent an animal blastomere from contributing to the retina. However, increasing bone morphogenetic protein (BMP) signaling in the retina-producing blastomeres significantly reduces their contribution. Conversely, reducing BMP signaling by expression of a dominant-negative BMP receptor or Noggin allows other animal blastomeres to contribute to the retina. Thus, the initial step in the retinal lineage is regulated by position within the BMP/Noggin field of epidermal versus neural induction. Vegetal tier blastomeres, in contrast, cannot contribute to the retina even when given access to the appropriate position and signaling fields by transplantation to the dorsal animal pole. We tested whether expression of molecules within the mesoderm inducing (activin, FGF), mesoderm-modifying (Wnt), or neural-inducing (BMP, Noggin) pathways impart a retinal fate on vegetal cell descendants. None of these, several of which induce secondary head structures, caused vegetal cells to contribute to retina. This was true even if the injected blastomeres were transplanted to the dorsal animal pole. Two pathways that specifically induce head tissues also were investigated. The simultaneous blockade of Wnt and BMP signaling, which results in the formation of a complete secondary axis with head and eyes, did not cause the vegetal clone to give rise to retina. However, Cerberus, a secreted protein that also induces an ectopic head with eyes, redirected vegetal progeny into the retina. These experiments indicate that vegetal blastomere incompetence to express a retinal fate is not due to a lack of components of known signaling pathways, but relies on a specific pathway of head induction.

Activins↗
PubMed1996

Surviving the chaos of merger mania.

Mergers are the watchword of the decade as managed care changes how health care is delivered. Beyond changing day-to-day operations, mergers can affect staff personally. How can home care and hospice managers help their staff to keep priorities straight and morale high?

Delivery of Health Care, Integrated↗
PubMed1990

Silver-silver chloride plunge electrode needles and chloriding monitor.

A plunge electrode is made from a hypodermic needle with one side cut open and multiple electrodes exposed from tip to base. A method for constructing chlorided silver electrode plunge needles is explained as well as problems associated with electrode chloriding. The small surface area of these electrodes makes empirical methods of chloriding difficult to use. A monitor was constructed for the testing and chloriding of a twelve-electrode plunge needle. This system continuously measures the impedance of the electrodes during chloriding.

Electric Conductivity↗
PubMed1987

Necessity and methods of HTLV-III inactivation in contact lens practice.

This paper reviews and analyzes the sensitivity of HTLV-III to various agents. The finding of HTLV-III in tears, the conjunctiva, and the cornea indicates the remote possibility that acquired immunodeficiency syndrome (AIDS) can be spread by instruments in contact with the eye, specifically trial contact lenses. Common contact lens disinfection systems are compared to agents known to inactivate HTLV-III. Recent studies reveal that heat disinfection may not be adequate, thereby, leaving only H2O2 systems as a potentially effective method of inactivating large titers of the virus. Other possible disinfection methods are proposed based on known sensitivity of HTLV-III but are awaiting further investigation.

Acquired Immunodeficiency Syndrome↗